Fig. 7: SLC43A3 protects against PA-induced lipid accumulation and cell senescence through the ER-stress pathway. | Communications Biology

Fig. 7: SLC43A3 protects against PA-induced lipid accumulation and cell senescence through the ER-stress pathway.

From: Palmitic acid induces lipid droplet accumulation and senescence in nucleus pulposus cells via ER-stress pathway

Fig. 7

a IF staining of GRP78 and Chop in NP cell. Scale bar: 10 µm. b BODIPY staining for lipid droplets. Scale bar: 10 μm. c, d Oil red staining for lipid droplets. Scale bar: 100 μm. The positive oil red staining cells are shown in the statistical chart; n = 3. **P < 0.01. e Ultrastructural view of lipid droplets using TEM. Scale bar: 0.5 μm. f, g IF staining of P53, P21, P16, and RB. Scale bar: 50 μm. h EdU staining detected the proliferation of NP cells. Scale bar: 100 μm. i Representative SA-β-gal staining of NP cells. Scale bar: 100 μm. j, k The positive EdU- and SA-β-gal cells are shown in the statistical chart. n = 3. **P < 0.01; ***P < 0.001. l Schematic representation of the mechanism. Abnormal PA accumulation was detected in IDD, resulting in lipid droplet accumulation and cell senescence in an endoplasmic reticulum stress-dependent manner. Overexpression of SLC43A3 significantly alleviated PA-induced endoplasmic reticulum stress, lipid droplet accumulation, and cell senescence by inhibiting PA uptake.

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